The objective of the proposed investigation is directed toward elucidating the mechanisms by which estrogens, through other mediators, regulate blood flow through the uterine vascular bed. Prostacyclin (PGI2) appears to play a significant role as a mediator in this process, and we have shown it to be a potent uterine vasodilator. We will study the effects of prostacyclin synthetase inhibition on estrogen-induced uterine blood flow and uterine vascular resistance. In addition, we will measure the uterine production rates of thromboxane B2 and 6-keto-PGF1 alpha in response to estrogen stimulation with and without PGI2 synthetase inhibition. Finally, we will explore the inter-relationship of cycloheximide on adenosine and arachidonic acid-induced increases in uterine blood flow.